Mutual regulation between β-TRCP mediated REST protein degradation and Kv1.3 expression control vascular smooth muscle cell phenotype switch

Phenotypic switch of vascular smooth muscle cells (VSMC) plays a key role in the pathogenesis of atherosclerosis and restenosis after artery intervention. Transcription repressor element 1-silencing transcription factor (REST) has been identified as key regulator of VSMC proliferation. In the present study, we sought to investigate the potential association of E3-ubiquitin ligase β-TRCP mediated REST protein degradation with Kv1.3 expression during VSMC phenotypic switch.

Source: Atherosclerosis - August 28, 2020 Category: Cardiology Authors: Meng Ye, Xiangjiang Guo, Han Wang, Yuli Wang, Xin Qian, Haoyu Deng, Weilun Wang, Shuofei Yang, Qihong Ni, Jiaquan Chen, Lei Lv, Yiping Zhao, Guanhua Xue, Yinan Li, Lan Zhang Source Type: research